Alzheimer’s disease (AD) is a disorder that has defied practically everything that researchers have done to find a cure. A change in approach may be all that is needed to record success, according to a study.
Alzheimer’s is a really disturbing condition that is hard to manage, with no proven means of prevention available yet. Its incidence has been rising and looks to continue that way for years to come.
There are about 5.5 million cases in the U.S. as of 2018, according to the Alzheimer’s Association. The lack of effective means of prevention raises the fear that the incidence will continue to increase. It is projected that almost 14 million Americans will have the disorder by 2050.
Currently available treatments offer limited benefits and are costly. Trials after trials on new drugs for the disorder have failed.
It is long-believed that Alzheimer’s is the result of the accumulation of beta-amyloid plaque or Tau protein in the brain. But no research has conclusively shown that this buildup is responsible for the anomaly.
In a research paper that was published in Neuron in July, Dr. Joel Dudley, associate professor of Genetics and Genomic Sciences at Icahn School of Medicine at Mount Sinai Hospital, New York, and his colleagues indicated that viral infections may be a possible trigger.
The study highlighted the possible usefulness of approaching Alzheimer’s research from different angles.
Years of failures
The treatment for Alzheimer’s disease is limited today not for lack of effort, but because of failed attempts for years. Researchers have tried time and again to come up with an effective drug, but ended up getting frustrated.
A good example of these frustrating outcomes is that of Intepirdine acquired by Axovant Sciences from GlaxoSmithKline in 2014. The clinical-stage pharmaceutical company ended up with poor results after raising around half a billion dollars to carry out trials on the drug.
Over a year before then, Eli Lilly had announced negative results from trials on the drug Solanezumab.
Practically all drugs approved for trials from 2002 to 2012 returned with unimpressive results.
Linked to viruses?
The research by Dudley and colleagues suggested that viral infection may have a connection to the development of Alzheimer’s diseases.
It has long been suspected that pathogenic microbes might play a role in the development and worsening of Alzheimer’s disease.
In the “Multiscale Analysis,” the researchers tried to see if they can find a connection between the disorder and different types of viruses. This led them to observe that there might be a relationship between Alzheimer’s and human herpesviruses 6A (HHV6-A) and 7 (HHV-7). It was found that the brains of deceased people with Alzheimer’s had higher levels of these herpes viruses than control subjects.
The findings didn’t necessarily mean that these microbes directly cause AD. The hypothesis is that they induce an immune response that, in turn, results in a buildup of beta-amyloid, possibly to protect the brain.
What this means basically is that beta-amyloid is more of a response to the dreaded brain disorder and not the cause.
A change of tactic
This study displays the need for flexibility in the manner of approach to Alzheimer’s drug research. All this while, researchers have practically worked with the view that the condition results from beta-amyloid plaque buildup. Anybody that thought otherwise wouldn’t be taken seriously.
A different approach to research may help bring about a reduction in costs. Estimates show that the treatment of dementia, including Alzheimer’s, will cost about $277 billion this year alone.
Working on the theory that beta-amyloid plaque is responsible for Alzheimer’s disease, hasn’t brought much progress in drug development. Trying something different will likely not hurt.